Evidence map›Paper›PMID 24481326›Full record

ReviewEndocrine-related cancer2014

Genetically engineered ERα-positive breast cancer mouse models.

Sarah A Dabydeen, Priscilla A Furth

Abstract readReview
In one paragraph

Review in Endocrine-related cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Rat Models of Hormone Receptor-Positive Breast Cancer.Journal of mammary gland biology and neoplasia · 2024
    Review
  6. Article
  7. Advances in Immunocompetent Mouse and Rat Models.Cold Spring Harbor perspectives in medicine · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Mammary adipose stromal cells derived from obese women reduce sensitivity to the aromatase inhibitor anastrazole in an organotypic breast model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  19. Homology models of mouse and rat estrogen receptor-Computational toxicology (Amsterdam, Netherlands) · 2019
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Sarah A DabydeenDepartments of Oncology Medicine, Lombardi Comprehensive Cancer Center, Georgetown University, 3970 Reservoir Road NW, Research Building, Room 520A, Washington, District of Columbia 20057, USA.
Priscilla A Furth

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI Louis M Weiner · 1990 to 2026
$71.5M
TRAINING GRANT IN TUMOR BIOLOGYT32CA009686 · NCI · GEORGETOWN UNIVERSITY · PI ANNA Tate RIEGEL, DAVID J ROBBINS · 1996 to 2026
$10.8M
Progression and regression of mammary preneoplasiaR01CA112176 · NCI · GEORGETOWN UNIVERSITY · PI FURTH, PRISCILLA A. · 2005 to 2018
$3.1M
NCI NIH HHS 1R01CA112176NCI NIH HHS 5P30CA051008NCI NIH HHS 5T32CA009686NCI NIH HHS P30 CA051008NCI NIH HHS R01 CA112176NCI NIH HHS T32 CA009686
6 · The paper itself

Abstract

The majority of human breast cancers are estrogen receptor-positive (ER+), but this has proven challenging to model in genetically engineered mice. This review summarizes information on 21 mouse models that develop ER+ mammary cancer. Where available, information on cancer pathology and gene expression profiles is referenced to assist in understanding which histological subtype of ER+ human cancer each model might represent. ESR1, CCDN1, prolactin, TGFα, AIB1, ESPL1, and WNT1 overexpression, PIK3CA gain of function, as well as loss of P53 (Trp53) or STAT1 are associated with ER+ mammary cancer. Treatment with the PPARγ agonist efatutazone in a mouse with Brca1 and p53 deficiency and 7,12-dimethylbenz(a)anthracene exposure in combination with an activated myristoylated form of AKT1 also induce ER+ mammary cancer. A spontaneous mutant in nude mice that develops metastatic ER+ mammary cancer is included. Age of cancer development ranges from 3 to 26 months and the percentage of cancers that are ER+ vary from 21 to 100%. Not all models are characterized as to their estrogen dependency and/or response to anti-hormonal therapy. Strain backgrounds include C57Bl/6, FVB, BALB/c, 129S6/SvEv, CB6F1, and NIH nude. Most models have only been studied on one strain background. In summary, while a range of models are available for studies of pathogenesis and therapy of ER+ breast cancers, many could benefit from further characterization, and opportunity for development of new models remains.

Indexed as

Disease Models, AnimalAnimalsBreast NeoplasmsEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHumansMiceEstrogen Receptor alphabreastcarcinomaestrogen receptormammary glandpathogenesis

Identifiers

PMID24481326
PMCPMC4013173

What OpenQuestion holds

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.